A P P E N D I X A
What About the Widely Advocated Dietary Restrictions on Fat, Protein,
and Salt, and the Current High-Fiber Fad?
*A 1995 article in the journal Nutritional Biochemistry, 6:411–437,
demonstrated that a higher protein diet enables the kidneys to increase
their capacity for net acid secretion as ammonium.
Studies on diabetic rats have shown the following: Rats with blood
sugars maintained at 250 mg/dl rapidly develop diabetic nephropathy
(kidney disease). If their dietary protein is increased, kidney destruction
accelerates. At the same laboratory, diabetic rats with blood sugars
maintained at 100 mg/dl live full lives and never develop nephropathy,
no matter how much protein they consume. Diabetic rats with high blood
sugars and significant nephropathy have shown total reversal of their
kidney disease after blood sugars were normalized for several
months.
Other studies have enabled researchers to piece together a scenario
for the causes of diabetic nephropathy, where glycosylation of proteins,
abnormal clotting factors, abnormal platelets, antibodies to glycosylated
proteins, and so on, join together to injure glomerular capillaries.
Early injury may only cause reduction of electrical charge on the pores.
As a result, negatively charged proteins such as albumin leak through
the pores and appear in the urine. Glycosylated proteins
leak through pores much earlier than normal proteins. High blood pressure,
and especially high serum insulin levels, can increase GFR and force
even more protein to leak through the pores. If some of these proteins
are glycosylated or glycated, they will stick to the mesangium, the
tissue between the capillaries. Examination of diabetic glomeruli indeed
discloses large deposits of glycated proteins and antibodies to glycated
proteins in capillary walls and mesangium. As these deposits increase,
the mesangium compresses the capillaries, causing pressure in the capillaries
to increase (enlarging the pores) and larger proteins to leak from the
pores. This leads to more thickening of the mesangium, more compression
of the capillaries, and acceleration of destruction. Eventually the
mesangium and capillaries become a mass of scar tissue. Independently
of this, both high blood sugars and glycated proteins cause mesangial
cells to produce type IV collagen, a fibrous material that further increases
their bulk. Increase in mesangial volume has been found to be commonplace
in poorly controlled diabetes even before albumin or other proteins
appear in the urine.
Many studies performed on humans show that when blood sugars improve,
GFR improves and less protein leaks into the urine. When blood sugars
remain high, however, there is further deterioration. There is a point
of no return, where a glomerulus has been so injured that no amount
of blood sugar improvement can revive it. Although this seems to be
true for humans, blood sugar normalization has actually brought about
the appearance of new glomeruli in rats.
Nowadays many diabetics who have lost all kidney function are treated
by artificial kidneys (dialysis machines) that remove nitrogenous wastes
from the blood. In order to reduce the weekly number of dialysis treatments,
which are costly and unpleasant, patients are severely restricted in
their consumption of both water and dietary protein. Instead of using
large amounts of carbohydrate to replace the lost calories, many dialysis
centers now recommend olive oil to their diabetics. Olive oil is high
in monounsaturated fats, which are believed to lower the risk of heart
disease.
Because the survival rate of diabetics on dialysis is so much lower
than that of nondiabetics, some dialysis centers are now using low carbohydrate,
high-protein diets for their diabetic patients.
In summary: Diabetic nephropathy does not appear if blood sugar is
kept normal. Dietary protein does not cause diabetic nephropathy, but
can possibly (still uncertain) slightly accelerate the process once
there has been major, irreversible kidney damage. Dietary protein has
no substantial effect upon the GFR of healthy kidneys, certainly not
in comparison to the GFR increase caused by elevated blood sugar levels.*
The May 1996 Journal of the American Medical Association published
a summary of fifty-six studies demonstrating that in nondiabetics increased
protein consumption actually lowered blood pressure.
RESTRICTIONS ON SALT INTAKE: ARE THEY REASONABLE FOR ALL DIABETICS?
Many diabetics have hypertension, or high blood pressure. About half
of all people with hypertension will experience blood pressure elevations
when they eat substantial amounts of salt for at least two months. This
rarely occurs in those who are not already hypertensive. Hypertension
accelerates glomerulopathy (destruction of the glomerulus) in people
with chronically elevated blood sugars, but in type 1 diabetes, hypertension
usually appears after, not before, the appearance of kidney damage as
indicated by significant amounts of albumin in the urine. Is it therefore
appropriate to ask all diabetics to lower their salt intake?* Let us
look at a few of the mechanisms involved in the hypertension that some
diabetics experience.
*Your physician might find informative the following articles on this
subject:
“Molecular and Physiological Aspects of Nephropathy in Type 1 Diabetes
Mellitus,” by Raskin and Tamborlane, Jnl Diabetes and Its Complications,
1996, 10:31–37; “The Effects of Dietary Protein Restriction and Blood
Pressure Control on the Progression of Chronic Renal Disease,” by S.
Klahr et al., New England Jnl Med, 1994, 330:877–884; also, in the same
issue of New England Jnl Med, the editorial
“The Role of Dietary Protein Restriction in Progressive Azotemia” (pp.
929–930). Another study, in the journal Diabetes Care, 25:425–430, in
the year 2000, showed that obese people on a high-protein diet lost
more fat and less muscle mass than those on a low-fat diet. They also
showed more than double the reduction in LDL (the “bad” cholesterol).
People with advanced glomerulopathy will inevitably develop hypertension,
in part because GFR is severely diminished. These people cannot make
enough urine, and therefore retain water. Excessive water in the blood
causes elevated blood pressure. There are many other ways hypertension
can be caused by high blood sugars. The mere presence of high blood
sugar will cause water to leave tissues and enter the bloodstream, even
experimentally in nondiabetics.
It is not unusual to observe reduction in blood pressure concomitant
with control of blood sugar. Studies have shown that many, and possibly
most, hypertensive nondiabetics are insulin-resistant, and therefore
have high serum insulin levels. In addition to causing elevation of
serum triglycerides and reduction in serum HDL in nondiabetics, high
serum insulin levels have long been known to foster salt and water retention
by the kidneys. Furthermore, excessive insulin stimulates the sympathetic
nervous system, which in turn speeds up the heart and constricts blood
vessels, causing further increase in blood pressure. Thus type 2 diabetics
who eat lots of carbohydrate, and therefore will tend to make excessive
insulin, can readily develop hypertension. Type 1 diabetics treated
with the usual industrial doses of insulin to cover high-carbohydrate
diets are likewise more susceptible to hypertension. One dramatic study
showed that in hypertensive individuals, blood pressure is directly
proportional to serum insulin level. A report from Nottingham, England,
showed that a brief infusion of insulin and glucose would increase blood
pressure in normal men without changing their blood sugars. A 1998 study
in Glasgow, Scotland, demonstrated that salt restriction increased insulin
resistance in type 2 diabetics.
*A study of older individuals who were rotated between low-, moderate-,
and high-salt diets demonstrated that those on low-salt diets experienced
significantly more sleep disturbances, and had more rapid heart rates
and higher serum norepinephrine (adrenaline) levels. An international
study called Intersalt, covering 10,079 people in 32 countries, reported
in 1988 that “salt has only small importance in hypertension. ”More
recently, another study showed that salt restriction increases insulin
resistance and thus can indirectly increase blood pressure. Large amounts
of dietary salt can facilitate loss of calcium from bones of post-menopausal
women, who are already at high risk for osteoporosis (bone weakening).
Why don’t all diabetics on high-carbohydrate diets or all poorly controlled
diabetics have hypertension?
One reason is that the body has several very efficient systems for
unloading sodium (a component of salt) and water. One of the more important
of these systems is controlled by a hormone manufactured in the heart
called atrial naturietic factor (ANF).When the heart is expanded by
even a slight fluid overload, it produces ANF. The ANF then signals
the kidneys to unload sodium and water. Hypertensive individuals, and
the children of two hypertensive parents, tend to produce much lower
amounts of ANF than do normal people. Nonhypertensive
diabetics apparently are able to produce enough ANF to control the blood
pressure effects of high blood sugars and high serum insulin levels,
provided they do not have moderately advanced kidney disease. Indeed,
a study, in which some of my patients participated, showed that diabetics
with high blood sugars produce significantly more ANF than those with
lower blood sugars.
How does all this apply to you? First, you and your physician should
know if you have glomerulopathy. This is readily determined if the renal
risk profile tests suggested in Chapter 2 are performed. If these tests
are abnormal, your physician may advise you to reduce your salt intake
because salt is much more likely to cause hypertension in people with
diminished GFR.
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